It's Not Cholesterol. Inflammation Is What's Actually Causing Heart Disease

Why are we still seeing so many people with heart disease?

Yeah, it's still the number one killer around the world, not just here. And it's still the number one killer in women who, you know, they think that it's breast cancer. No, no, it's— this is it.

I concluded that one of the root causes, Mark, was this flawed hypothesis that we should have low-fat diets to prevent heart disease.

Cardiovascular disease is an inflammatory process, that it's not just about cholesterol, but there's ongoing inflammation.

Chronic stress. Loneliness, isolation, bad sleep— those things are huge in heart disease.

But we know that 80% of cases of heart disease and diabetes may actually be preventable with diet and lifestyle.

As part of our summer series, we're revisiting some of the most important conversations we've had on the topics that matter most to our health, and few are more important than heart disease. Heart disease remains the number one cause of death worldwide, and despite decades of research, millions of prescriptions, and billions of dollars spent on treatment, many people still are confused about what actually causes it and what we can do prevent it. For years, the conversation on heart disease has focused almost entirely on cholesterol. But what if that's only part of the story? In this compilation episode, you'll hear from Dr. Cindy Geyer of the Ultra Wellness Center, Dr. Eric Topol, and Dr. Seemal Hotra as they explore a different perspective on heart disease, one that goes beyond cholesterol and looks at the deeper drivers of cardiovascular risk, including inflammation, insulin resistance, metabolic dysfunction, lifestyle, and and early detection. You'll hear why many experts now believe that heart disease often begins decades before symptoms appear, why traditional testing can miss important signs and— that are warning signs, and how emerging science is giving us new tools to identify risk earlier than ever before. And more importantly, you'll hear a message that is both practical and hopeful, and that many of the factors driving heart disease are within our control, and that prevention remains one of the most powerful tools we have. So let's dive in.

So let's talk about heart disease, 'cause we think we know all about heart disease. Oh, it's cholesterol and statins are the cure. And if that doesn't work, you get a bypass and angioplasty. And you know, if that doesn't work, you get a heart transplant. That's sort of, and then, you know, of course there's all the normal causes we know, like diabetes and high blood pressure and high cholesterol. But diabetes is a symptom. High cholesterol's a symptom. Smoking's a habit. And Yet we're kind of missing the boat, I think, on a lot of the reasons we have heart disease and what we can do about it from a, a more systems perspective. So let's talk about, um, just what a big deal this is and, and how few people actually are meeting the simple behaviors that will prevent heart disease.

Yeah.

Again, this is another one of those conditions that the debate is, well, it's in my family, so I'm doomed to get it. But we know that 80% of cases of heart disease and diabetes may actually be preventable with diet and lifestyle. And despite that really powerful message, fewer than 3% of the US population is meeting the core 4 basic characteristics that predict low risk. And it's a pretty low bar, Mark.

And what are those?

What are those 4 things?

It's not smoking.

Okay.

Getting the minimum recommended 150 minutes of exercise a week, eating in the top 2 quintiles of what's considered a whole foods diet, and having a healthy body fat percentage. Fewer than 3%. I still find that shocking.

So not too much body fat, eating pretty healthy, little exercise, and don't smoke.

Yeah.

That's it. Simple things to do, but like—

We're not even there yet.

3%.

Yeah.

3%.

And what's really staggering is that, you know, not only do people not meet those habits, but that there are some really other big factors that we are just so bad at in America. Our whole society is set up to actually cause heart disease.

Absolutely.

What are those things that, that really are these risk factors that besides cholesterol?

Well, of course it's inflammation. I mean, you and I were working together back at Canyon Ranch when that pivotal study came out. I think it's been 21 years or so.

I remember that New England Journal of Medicine review paper. Yes.

Peter Libby and Paul Ridker.

Yeah.

Showing that cardiovascular disease is an inflammatory process.

Yeah.

That it's not just about cholesterol, but there's ongoing inflammation. And as you've talked about many times on this podcast, inflammation is not— it's also a symptom that it can come from a lot of different places. Because in our paper, our local paper, when that article came back out, I don't know if you remember this, it said President Bush's doctors measured his CRP, which is the common marker of inflammation, and they don't know what to do about it.

Right, right.

So it's one thing to say, well, we know inflammation matters. It's another one entirely.

Take aspirin.

Take aspirin and a statin, right? But it's another to say, well, what are the root causes of inflammation?

Well, that's true. And we, there's a lot of them. And some of the things that we don't typically think of as causing inflammation, we know infections and allergens and things like that, even toxins and bugs in your gut, but stress causes inflammation.

Absolutely.

Lack of exercise causes inflammation.

Yeah.

Bad sleep causes inflammation. Loneliness and isolation cause inflammation, and those are pandemics.

Yes.

In America. Chronic stress, loneliness, isolation, bad sleep. I mean, those things are huge in heart disease and we often miss, miss the boat on helping our patients really deal with those.

Right.

So, okay. So the typical person comes in, he's got a high cholesterol. He or she is a high risk for heart disease, maybe family history. Typical doctor does, sort of what workup and, and what kind of treatments?

So a typical doctor might measure a glucose and an A1C to look at their blood sugar status, and they would do a standard cholesterol profile, which interestingly enough calculates your LDL cholesterol, the one we usually think of as being the lousy cholesterol, from a formula, doesn't even really measure it, and base most of the decisions on that.

Mm-hmm.

If they have symptoms, they might send 'em to a cardiologist for a stress test.

If they have chest pain.

If they have chest pain, right.

Or shortness of breath on exercise. It's already kind of down the road, right?

Um, but most doctors don't measure C-reactive protein because as I mentioned before, it's like, well, what do we do with it?

What do I do with it?

What do I do with it? Oh, statin and aspirin. And then they're probably gonna treat 'em with, if they are pre-diabetic or diabetic, they're gonna give them metformin or medications to lower blood sugar and probably a statin to control the cholesterol. How often do they actually talk to them about those root causes such as diet and stress and sleep? Maybe not.

Yeah.

They're talking about this polypill as a treatment, which is this combo pill of an aspirin, a statin, and a blood pressure drug.

Yes. Put it in the water.

Just like give it to everybody. It'll prevent heart disease. I'm like, yeah, okay. Well, why do we have high blood pressure? Why do we have an aspirin? A need for aspirin and inflammation? Why is our cholesterol all screwed up? Yeah.

And you know, it's really interesting. There's, believe it or not, there's a potential behavioral component for patients who go on a statin and their cholesterol's now normal. It's good.

Oh yeah.

I can eat my cheeseburger.

I can eat my cheeseburger.

My fried chicken.

Isn't that interesting that people change their diet in an unhealthy way?

Oh yeah.

When their numbers better.

One of the worst things I ever read was there was a bunch of cardiologists advocating for selling statins over the counter at McDonald's and fast food restaurants.

Oh my gosh.

And I think they do sell even statins over the counter and it's like those commercials for the acid blockers, like, "Take some Pepcid 'cause don't worry, Daddy, you can eat your peppers and sausages.

Just take the Pepcid." I remember that.

And I was like, "No, don't eat the peppers and sausage." So, you kind of mentioned they do sort of a cholesterol profile, but there was a hint of a subtext in that sentence where they really weren't measuring the right thing.

Yeah.

So we tend to look at things that we're used to looking at that are easy to test and measure. But, you know, one of the things that I think people forget, and I think doctors honestly forget, is we get trained in this panel of tests and it's your blood count, your metabolic profile, and your cholesterol. And we measure like a few things, maybe it's 30, 40 things. Maybe if like it's a super fancy doctor, they'll measure 100 things. Like, and they think they're kind of checking everything. Oh, your tests are fine. Everything's great. You look good. And the truth is that, uh, they're missing a huge amount. There are literally tens of thousands of different molecules in your body, all doing things all the time, every minute, every second. And we ignore most of them. And they, we, in fact, we may ignore some of the most important ones.

And when it comes to cholesterol, we've covered this on the podcast with Dr.

Bohm. We went really deep into this and we just should just do a quick refresher. Because the test that most people get, not the one we get here at the UltraWellness Center, but the test that most people get is like an antiquated cholesterol test that doesn't really tell you a whole lot. And I have a patient yesterday who was a classic example of that, right? So tell us about, and I'll tell you about his test in a minute, but tell us about your, you know, the new kind of testing that we're doing. It's not so new because we've been doing it for 20 Right. But, but, and the, and the discovery that allowed for the testing was, oh, 50 years ago.

Yeah. So, so the focus has been on amount of cholesterol, but we wanna know the quality of the cholesterol. So we know, for example, LDL, that's typically labeled the lousy cholesterol. There's big fluffy puffy pattern A LDL cholesterol, which is less easily made into a plaque in the artery, less prone to inflammation and oxidative stress and rupture. So it's a less risky LDL, whereas somebody could have small dense pattern B LDL, and that's the really risky LDL. So quality matters. And if you have two people with a calculated LDL of 130, one of 'em could all have pattern A low-risk LDL and they're actually fine. Somebody else could have lots of those dense particles that's not captured by the calculated LDL of 130. So the quality matters. The same's true for HDL. We've historically thought of HDL as being the good healthy cholesterol, but size matters there too. Small HDL doesn't seem to be as able to cart out the bad LDL and get rid of it. So we want to know the quality and the size of both the HDL and the LDL, and we want to know what other remnant particles are floating around, like very low density lipoprotein and intermediate density lipoprotein, and those don't show up on a typical panel.

Yeah, so, so, so practically what you see is people come in with when it looks like a normal cholesterol. Like this guy yesterday has early dementia. His cholesterol I think was 160-something.

Sounds good.

Yeah. His LDL was, I think, under 100. Triglycerides weren't bad. His HDL was 39, which is kind of low. But we looked at his particle number, even though his LDL, like if your regular doctor, "Oh, that's a great 160. That's a great cholesterol." They missed the boat because his particle number was, was like 1,500. It should be under 1,000.

Wow.

And his small particles, which should be like zero or less than 300 is, you know, you can live with, but anything over that is high. His was 900.

Wow.

So he was like, and he was a skinny older guy, was 84 years old and had, you know, lost muscle, belly fat, you know, underweight, over fat. And he was pre-diabetic and that was driving some of his dementia. But they would go, oh, your cholesterol's fine. Not an issue. And, and we also look at a lot of other things besides that. And by the way, you know, in 2021, no one should get the regular cholesterol panel. I mean, you, you gotta insist from your doctor. You can get it from LabCorp Quest called NMR or Cardio IQ. It's, it's so important to do. And, and I guess, you know, the problem is most doctors won't know what to do with it once they find it. There's no drug for it. Like, oh, your LDL's high, we'll give you a statin. It's like we treat what we can easily test and find, not necessarily what the right thing is. And so with heart disease, you know, it really is a metabolic issue. It's, you know, they shouldn't be called cardiologists, they should be called cardioendoimmunologists, right? Because it's all about the hormones, including insulin, and all about the inflammation, immune system. And you mentioned earlier that study by Paul Ridker and Libby in which it was sort of the beginning of the conversation. A lot of the follow-up studies like the Jupiter trial, they found that if patients had a high LDL but they didn't have a high CRP, their risk of heart disease was negligible. But if they had a high LDL and a high CRP, that was the problem. So independent of inflammation may not be an issue.

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And also you can get falsely confused by cholesterol tests. You've seen these patients who were, and I don't mean to stereotype people, but like it was this kind of cohort of women who are probably in their 70s and 80s who are thin, who are fit. The ladies we see at Canyon Ranch who like exercise, eat well, don't smoke, normal blood pressure, no diabetes, and their cholesterol is 300 and their HDL is 100 and their LDL is like, I don't know, maybe 150 or something. And they have no small particles and they have all these large fluffy things and they're in really no risk for heart disease.

And they don't need a statin.

Right?

Right. I even asked Peter Libby, who's the chair of cardiology at Harvard, like, do these women need a statin? And they're like, no, they don't. We don't have any data to say that they do.

And I'm like, oh, that's interesting.

So we kind of have to be really personalized in our approach.

Yes.

And that's the other feature of functional medicine. Not like one size fits all. Everybody gets the poly pill. Everybody gets a statin, aspirin, and blood pressure pill. Like, no, we have to start to think about what's the cause. And heart disease is a symptom. It's a syndrome. It doesn't— there are many, many causes. So let's talk about this whole idea of metabolic health. Because, you know, we were chit-chatting a little earlier and it's staggering to me as a physician just how poor our metabolic health is. So, so how, how, how healthy are Americans metabolically?

Yeah, not very. So, so a recent study was looking at the NHANES data from 2009 to 2016.

Government surveys.

Government survey.

Our blood tests and health records and everything.

Right.

And trying to say, well, how many people are what we would call metabolically healthy? And if you're not familiar with it, for people who may not be familiar with that term, sort of meeting the optimal numbers for a blood pressure less than 120 over 80, HDL levels being in the high range, a good range, greater than 40 for men and 50 for women, having triglycerides that are low. Having a glucose that's less than 100. And they found that 12.12% of Americans, 12.2%, 12.2%, thank you.

12.2% of Americans were metabolically healthy, which kind of means that almost 88% of Americans are metabolically unhealthy. And since 75% of people are overweight, there's another 13% there. Yes. It's like, what are the, what's, what's going on with the skinny people?

Well, and that's the interesting piece. Fewer than one-third of so-called normal weight people were metabolically healthy. So that's another really important message.

Oh, wait, wait, wait, wait, wait, wait, wait. Did you just say that two-thirds of skinny people are metabolically unhealthy?

Yes.

And have pre-diabetes-like syndrome?

Yes.

Two-thirds?

That's mind-boggling to me. Wow.

Okay. So that means that what, like 95% of Americans are metabolic—

No, no, no. It's still the 88%.

Oh, 88%.

All right, all right.

Good, good, good. But they were looking at how strongly it correlated with weight.

Oh my God.

That's so terrible.

So just having a body mass index that's less than 25 is not a guarantee that metabolically healthy.

So if you're a skinny sugar and bagel eater, don't think it's fine because you're skinny.

Exactly.

Is basically the bottom line.

Exactly. Because foods have other impacts besides just what they do with cholesterol anyway. Foods directly impact the elasticity of the arteries, for example, which is another key player.

You mean food is more than calories, Cindy?

Food is information, Mark. You've said that for years. It talks to our genes. It talks to our systems.

Yeah.

Yeah.

Wow. So you're talking about how the food impacts our metabolic health and, and, and we're not really good at diagnosing metabolic dysfunction, right? I mean, 90%, I mean, okay, 1 outta 2 Americans has prediabetes or type 2 diabetes. And if you look at this new study, I would argue that 9 outta 10 Americans have some degree of prediabetes or type 2 diabetes, like 90% of Americans. So when you look at that data and you also look at the parallel data that 90% of Americans with prediabetes are not diagnosed by their doctor, right? That's terrifying, especially because this is a 100% reversible, preventable, treatable condition, and it gets worse and worse over time. And people just don't even know they have it. And doctors miss it because there's no pill to take. Oh, take metformin. Well, that's not gonna help, right? It's like, and, and so Um, what are the kinds of ways that we look at these patients differently? What are the tests that we do? What are the things that we really focus on when someone comes in with a risk of heart disease or they're concerned about heart disease? Mm-hmm. You know, what's our, what's our approach? It, it's not just looking at the typical cholesterol and even CRP.

Yeah.

So we would look at those, of course. We would also wanna know what is somebody's insulin. Most doctors measure glucose, but not insulin.

Mm-hmm.

I personally like to look at somebody's glucose trends over time, cuz if you think about something that's preventable, you don't wanna wait till they cross that threshold to prediabetes or diabetes. So even in the range of so-called normal glucose mark, um, you know this, somebody who's fasting glucose runs less than 85 is in a very different metabolic place than somebody who's fasting glucose is 95 to 99, even though they're both technically normal, that it's a spectrum of risk. And the farther along you march that spectrum, the higher the risk of heart disease and diabetes. So if somebody's glucose used to be 85 and then it was 91 and now it's 98, We're gonna talk to that person right off the bat about all the things they need to put into place to prevent it from progressing because they're already on that spectrum. So we also wanna know insulin levels, not just a fasting insulin, but sometimes the insulin response to food because the other thing that's emerged is insulin's a player and way before somebody's blood glucose goes up, they might be pumping out tons of insulin to try to keep it in a good place.

Mm-hmm.

Mm-hmm.

And insulin by itself contributes to inflammation and more weight gain around the middle, that visceral adipose tissue. So we want to know their insulin, both fasting and in response to a challenge.

So wait, wait, wait, are you saying that sugar, not fat, that's causing heart disease? And sugar, the thing that's driving the insulin? Because fat doesn't cause insulin spikes.

Well, there is some— I mean, fat is a player.

Fat by itself.

Fat by itself is a player.

If you eat fat with other food, it will, but— Yeah.

Yeah. And I would say that quality of fat does matter. And we can talk some more about that, but I think fat plays a role with artery elasticity, which is another component of vascular risk. Yeah.

So fried foods, trans fats, refined oils, those are nasty. Absolutely. And they do not help.

Absolutely.

But fat in itself, if it's made from whole food sources and nuts and seeds and avocados and olive oil—

Might actually be beneficial.

Actually beneficial.

Yeah.

Yeah.

So what you're talking about is a set of diagnostic tests that are so important but mostly ignored. So then the, particle size and number, which nobody's doing. And the second is not just measuring your blood sugar A1C, which may be perfect and you may be in really bad trouble, but measuring also insulin in response to drinking like a couple of Cokes, right? I have a patient, Cindy, that I remember who was at super high risk for heart disease. And she had, I mean, she looked like the Tasmanian Devil. I mean, she was just like a round apple ball like this. And her belly was just like this big thing. And I'm like, this woman is in big trouble. And she's inflamed, she's at high risk for heart disease, high blood pressure, diabetes. And I'm like, let's check her glucose tolerance test with insulin. And this is, you know, this is like 20-plus years ago and no one was like looking at this. Even today, no one's looking at this. It's like so, so hard.

I mean, it took 50 years from the time the guy said, hey, we should wash our hands before surgery for us to wash our hands.

McKinley died, President McKinley, because he got shot in the belly and the doctor, McBurney, stuck his finger in the wound to check it out without washing his hands. So that's crazy. It took 50 years from the time the guy said, let's do the stethoscope so we don't get lice jumping into the doctor's hair to start using the stethoscope because the doctor used to put their head on the patient. So it takes forever and we've been doing this. Anyway, this woman, I did this test. I gave her this drink. And it was the most shocking thing I'd ever seen. And it taught me so much about what we miss in medicine. Her blood sugar was perfect, like 80, like, and, and she took the sugar drink and it was like perfect. Like, like it never went over 110 after taking like the equivalent of 2 Coca-Colas. Oh, she's fine. Her A1C was perfect. Her insulin normally should be under 5 fasting and under like 25 or 30 after a drink. Her insulin was like 50 fasting.

Wow.

And like 250 after a drink. So her body was just pumping out insulin, which was making her hungry, slowing her metabolism, putting fat in her belly cells, which were basically inflammation factories and leading to this perpetual cycle. And she was able to lose 50 pounds like that when we cut out starch and sugar.

Wow.

And I just feel like, you know, that, that showed me so much cuz you can even do a normal glucose tolerance test.

And that looks perfect.

And if you were super hyperinsulinemic, you're gonna, you're gonna miss that patient's real problem.

And you know, it's interesting, Mark, because that scenario is also associated with that cholesterol profile we talked about.

Yes.

With the small dense LDL and, and, and low HDL and the sequelae that we usually link to diabetes, fatty liver, peripheral neuropathy, all these other organs that are affected. And it can happen with the high insulins alone before the sugars go up.

Yeah.

It's a metabolic imbalance.

Yeah. So that's really the take-home here is that in heart disease is really a hormonal issue around insulin and insulin resistance and an inflammation issue.

So let's talk about the, the heart circulation because people say, well, that story's been told. You know, we've got statins, we've got this piece of SK9 inhibitors, we're all good. Like, what's the big deal? What should we worry about? It's just all about LDL cholesterol. What's new?

Yeah.

What, what should we be looking at? What should we be thinking about? And, and, and why are, why are we still seeing so many people with heart disease?

Yeah. It's still the number one killer around the world, not just here. And it's still the number one killer in women who, you know, they think that it's breast cancer. No, no, it's, this is it. This is exciting because, uh, we do know the things that we've been reviewing for risk factors, but we have a way. To now establish the risk. Are they really high risk without— before they ever have heart disease, 20 years plus? And the way we do that is we can get a simple lipid panel, add the Lp, ApoB. So a little more than what is the standard lipid panel. The Lp will be part of a lipid panel in the next year or two. But anyway, when we get that, lipid panel, which is again, very inexpensive. And we can also get a polygenic risk score, very inexpensive. We can also get a heart clock, right? And we can get inflammation markers. Anyway, now you have the full stack with your records and, you know, and you have somebody who is well before they've ever manifest heart disease. And you say, oh wow, this person is really high risk for heart disease. What do we do? Well, you get their LDL down. You know, not just to below 70, we go down to 20 or, you know, 30, less than 30, right? We have so many ways to do that now. We have these injectables that are against this PCSK9. We've got new drugs, 5 new Lp drugs that are going to be out within the next year or so that are really potent.

And we've had none of them, none till now.

Yeah. We never had one. We always tell, well, too bad your Lp is over 100. You know, nothing we can do. We're going to be able to change that. And that's going to have a big impact. We can get all the inflammation, get all over it, right? In terms of bringing the inflammation down, uh, we've already seen how GLP-1 drugs do that before any weight loss. So that should work well in people who aren't even obese. And we've seen how that can prevent heart— preserve ejection fraction heart failure, which is half of all heart failure, right? GLP-1s prevent that. So for heart disease, we're seeing some really breakthroughs for the treatment, particularly the new target of LDL that we have 5 different drug classes, statins you've mentioned, but the, the PCSK9, we have 3 different ways to do that now. We got other new drugs that are coming. Uh, just recently the CETP inhibitor worked really well on top of, so we got we can stamp out inflammation. The other thing is we have a metric we never had before, which is AI. And by the way, that also goes with Alzheimer's. You can do a retina AI exam. So I have a picture of the retina and you do AI on it. And it tells you when you're going to have Alzheimer's, if you're going to have Alzheimer's, 5 to 7 years in advance. The retina also tells if you're going to have heart disease or stroke in advance. It will even tell if you're going to you know, your calcium score of your heart arteries through your retina. It's remarkable. And we should be— that should be widely available. It isn't yet, but it will be. We'll be doing smartphone retina checks someday, right? But here's where we get a real kick on, a jump on this, because if you are concerned about high risk and somebody, you know, say 40, 50, They have significant risk factors. You can do a CT angio, which is now becoming very inexpensive. And you can look at inflammation in the artery. I go through this in the book. Inflammations in the artery without a narrowing. Okay. So the, the, it basically does AI Mark of the fat around the artery. And it, and this is something that was developed in the UK and it's now getting ready for FDA approval. This is a big jump because we always were worried.

So this isn't the Cleerly scan. This is something else.

No, no. Cleerly and the other ones in the US don't do this, but this is a, uh, a Oxford University of Oxford spinout. I think it's called Karista. They're going to have that available soon. And I went through the data in the book. I mean, they've had multiple papers, but it's striking if you have inflammation without a narrowing. It's, you know, you, you could have 15-fold risk of a heart attack. So that's when you use that as a metric, just like we were talking about the P-tau 217 for Alzheimer's. Yeah.

Yeah.

We've got all these new things for cardiovascular. We are gonna get a, a grip on this and we gotta, you know, ideally start early. But, you know, the lifestyle factors work really well. This is the most preventable known of the 3 big age-related diseases. Through lifestyle.

Because even without a lot of the drugs, like the lifestyle plays a big role. Like, you know, I've seen data up to 90% by healthy diet, exercise, stress mitigation, sleep, right?

Yeah.

I mean, is that, is that— in the book, I found all these studies that I was really struck by that are recent that show that if we practice the lifestyle factors that we've been reviewing with the details that we just discussed, That gets us 7 to 10 years of healthy aging without one of these age-related diseases. I mean, who wouldn't want 7 to 10 years of healthy aging just from the stuff we've been discussing without any, you know, magic potion or pill? Uh, so that's, I think people don't know about that. I didn't know about that. It's really impressive.

That's powerful. So, so what you're saying is some of the advances in cardiology are more pharmacological that you're thinking are coming, like the drugs that lower this genetically determined lipoprotein called Lp, which I've been checking for 30 years. ApoB, which I've been checking for 30 years. I read some article the other day that was like, there's this great new test that can be more predictive of your risk of heart attack than any other test is just discovered. I'm like, what is that? I'm like, look, click through the article. It's like ApoB.

I'm like, oh God.

Yeah. I mean, I mean, you only, you only need to get it once and then you can tell that if you need to check it, uh, further. But you're getting at a key point here is it isn't just that we have better, you know, more armamentarium of drugs, but we didn't know how to get the risk down. You know, we didn't know how to say this person's really high risk for atherosclerosis because we didn't really have, we didn't use the polygenic risk score. We didn't have, as we do now, we're going to have a heart clock. We, we, so there's a big debate out there, as you probably know, How low should we go on LDL? Should we pull out all the stops? Well, if you look at all the data, the lower you go, the more protection, but you don't want to necessarily give people, you know, ezetimibe and a statin and an injectable and all these things, unless they really are at high risk. Then you go for broke and you also get the Lp and you get the inflammation down. We have ways that we can do that, and we're going to keep having better ways. So this is a striking, uh, it's a combination of who's at risk, partitioning the risk, and having better ways to work on that risk.

Just to play devil's advocate, because this conversation comes up all the time, you're a cardiologist, so your favorite organ is the heart. And so your idea is get the LDL as low as you can. Not everybody. But your brain is made up of a lot of—

Only in people who are at high risk.

In people who are at high risk.

Okay.

So if you're really high risk, but like, what about the effects, for example, on the brain and cognitive function? Because the, you know, cholesterol is a big part of your brain and sex hormones, which is what your testosterone is made from, is cholesterol. So how do you kind of navigate that? And what's the truth in what do we know?

Yeah. I mean, the statins are probably the most studied drug class, uh, in history, really. Some of the data that comes out of these big meta-analyses would say, oh, people don't get any leg cramps. That's not true. You and I know that's not true. People do get severe leg cramps where they can't even sleep at night, you know, and all sorts of other, you know, leg and muscle-related symptoms. Now, with respect to cognitive and sexual dysfunction, the data really don't show a hit there at all. And in fact, you know, I think that We have some data to suggest the chances of having dementia in people, and Alzheimer's, as you know, accounts for 70% of dementia, that if you, if you don't have the LDL lowered to, let's say, less than 100, less than 70, you're going to be at higher risk for dementia. So if anything, the data support statins. And, you know, the data for, well, sexual dysfunction. It's, again, some of that's vascular. And it mo— if it's vascular, we're talking about atherosclerosis. Uh, and that again is gonna be, uh, ameliorated with— and it, of course, we don't have to just rely on statins. A lot of people do have side effects from statins, no matter what the group at Oxford keeps saying that everyone can take a statin and it's just, you know, it's mental if they can't. When I wrote a, uh, when I wrote an op-ed in the New York Times, like a decade ago, and I called out the diabetes from statins. Okay. Because if you take a very potent statin, you have a higher risk of developing type 2 diabetes, right?

Yeah.

Oh, did I get slammed by my cardiology colleagues for that? I said, well, wait a minute, that's the data, folks. I'm sorry. And over the years, we've seen many more reports about, you know, the potent statins, high doses, where you get a higher risk. And you know what? Most physicians are not keeping up with this. They're not watching their patients to see if their glucose, like, oh, hemoglobin, you know, A1C or fasting glucose. And this is bothersome to me because that is a side effect of statins, particularly potent statins. So again, this is important because if we're going to lower LDL and pull out all the stops and, you know, high doses of Rosuvastatin, Crestor, or atorvastatin, Lipitor, that could also raise the risk of that person developing type 2 diabetes. We don't want to do that. And we have cardiologists, my colleagues, they are, you know, really sold on statins and they basically ignore this, this diabetes issue. And did I ever take grief?

No, I agree. I agree with you. And I think, I think there's, there's, um, a concern I have around its effect on mitochondrial function. And some of the data I've seen that even in people without muscle pain, even without elevated muscle enzymes, that there's mitochondrial damage on muscle biopsies. And for me, mitochondria are so key to healthy aging in the brain, in everything from Parkinson's to Alz— to, to heart disease, diabetes. Diabetics have poor, poorly functioning mitochondria. That may be part of why it causes it. And so I, I'm wondering, you know, some of these other drugs that are coming down the Pike, even though some of them are expensive, maybe a better solution.

Well, people that have clear-cut adverse effects, you know, the PCSK9 injectable drugs are a winner because they're potent. And they have not been associated with diabetes, which is really interesting. They have not been associated with cognitive or other side effects. So most insurers cover that now. We, you know, went through years where it was a Because they were so expensive, the cost has come down. So as long as people have the right indication where they have significant side effects or they need to have their LDL substantially lowered, it's usually not a financial stress for most people.

So heart disease, still it's lifestyle, but then there's a cocktail of other drugs in very high-risk patients that you can detect early to figure out. And, and what about lipoprotein fractionation, which is a lab test that we include as part of Function Health, as well as ApoB and Lp, something I've been testing for 30 years. But you think that's as important? Because to me, the particle number and particle size story is important, and it's a sort of a clue that there's insulin resistance, which is one of the biggest drivers of heart disease and all the other age-related diseases.

Yeah. I mean, I think it's, um, is mild, potentially mild incremental information. I just don't see that it has nearly the impact of just zeroing in on LDL and Lp, and I do recommend that everybody get an ApoB at least once. Uh, and then you can figure out whether that needs to be further assessed. These other things, you know, it's an additional expense. I just haven't seen the value, but, you know, I have colleagues that are lipidologists that test every known particle in mankind, right? I just haven't, I haven't really seen the benefit because it doesn't change usually To me, I got to know the person's risk, and then I'm going to go after inflammation. I'm going to work on their lifestyle, and if necessary, you know, get their LDL down as low as possible. So the other things just don't have a, for me, added value. But I do know there are people that are, you know, wild and crazy on every particle, small, large, dense, you know, you name it out there. Yeah.

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Yeah, so I hear you on that. I think it's, you know, sometimes more information isn't always better, but you know, then what is the most important information? I think you've covered that in your book. And I think, you know, we're going down the kind of the horsemen of the apocalypse, you know, the, the, the heart disease, the cancer, the dementia. I think diabetes is sort of all in there related, but you're talking about how there's kind of a newer, with the advances in our diagnostics, whether it's imaging or retinal scans or new ways we can measure dementia biomarkers we never had before, cancer we'll get into in a sec, that these diseases can become more optional. Like they're not inevitable. They, they don't have more agency than we ever had before, given what we know now. And when you layer up what we're learning with AI and using multimodal treatments, we'll be able to actually make a big dent if people really understood how to navigate this and The sad part is that, you know, you spend your time thinking about what's coming. Most physicians are just trying to deal with the onslaught of what is and don't have the bandwidth to actually apply this stuff until it kind of is way often decades later. And so I really appreciate your sort of paying attention to, you know, what's happening and keeping your nose to the scent of where things are emerging because otherwise people just don't know. And doctors, like you said, don't know. And And the average person doesn't know, but this is such a hopeful message. And I'd love you to sort of unpack how you came to go from being a trained cardiologist who basically swallowed the gospel.

Yep.

To one who understands and has looked at the literature and has come to a different conclusion because it's not just that you're anti-drug or you're anti-medical care, anti the system, you're for The truth and for science and for an objective look at the facts. So the question I have is, how did you go from being a trained cardiologist who believed in statins to one who started to question statins, to one who's come to understand that our approach to cardiovascular disease might be a little bit misguided? And we'll talk about what the right approach should be later, but I, I kind of wanna start with unpack, unpack the science for us. Cuz yeah, everybody listening has no, has heard if their cholesterol's high, to take a statin.

Sure.

And if statins cause side effects, which they do for a lot of people, probably 20% get some muscle damage or some symptoms or increase the risk of diabetes. You know, we'll talk about that data. There's still, there's still a huge drive in our society for prescribing these and globally.

Yeah, absolutely. So my interest in this came from really looking at the initially the obesity epidemic. So 2004, WHO announced it as an epidemic. You know, by 2010, I was then 9 years qualified as a doctor. I was specialist registrar in my cardiology training. I was seeing more people, this viscerally, I'm very sensitive to, how to put it, suffering around me, if you like, but also seeing my colleagues under more stress in the system. And I was like, hold on a minute, this, if we carry on down this trajectory, the whole healthcare system's gonna collapse. We won't be able to even manage people acutely if they are ill. Right. And I never thought that would happen. And ultimately that one of my own, two of my own pa— two of my parents both basically died because of failures in the system, because the system's under so much stress, right? Never predicted that would happen, but that's where I started from. And when I looked into the issue of obesity, you know, I concluded that one of the root causes, Mark, if not the main root cause, was this flawed hypothesis that we should have low-fat diets to prevent heart disease. Food industry exploited that increasing sugar intake, increasing refined carbohydrate intake. It became quite clear there was a clear correlation between that change in guidance in the late '70s in the US and early '80s in the UK. Yeah. When the obesity epidemic started to then, you know, take its trajectory down the wrong way.

Yeah.

And I covered a lot of this in my book, Eat Fat, Get Thin.

Yeah.

Which I, we sort of unpacked the whole history of how we got this low-fat craze.

Yeah.

And led to this high-sugar starch craze that then led to this dramatic rise in obesity, which now of course we're treating with another drug, the GLP-1 agonists and, you know, trisepatide and semaglutide or Ozempic and Wegyara. It's kind of crazy, right?

Yeah.

Just kind of flipped it upside down.

Oh, absolutely. So, so when I looked at that and started looking at the data and spending years and, and, and months and years looking at it and looking at different bits of data, I, I was able to put it all together and I wrote a piece in the BMJ in 2013 called Saturated Fat Is Not the Major Issue.

Right. I read it. That's how I first came across it.

Yeah. And that got a lot of attention, right? It was international news and British news and CNN International and whatever., you know, cuz obviously suddenly you've got a cardiologist busting this myth that we think butter has been bad for our cholesterol. But when I did that, okay, so what I looked at the data and it was very clear there was no clear association with saturated fat consumption and heart disease. So if that's true, then, and we know saturated fat raises LDL cholesterol, that means LDL cholesterol can't be that important. So, and if LDL cholesterol or total cholesterol isn't that important as a risk factor, how do statins work? But I knew statins had a, a separate effect to lowering cholesterol, which is their anti-inflammatory and their anti-clotting. And I knew this even, it's well known within even in cardiology circles. You know, I trained as an interventional cardiologist, and that means keyhole heart surgery, stents, for example. Patient comes in, we didn't even check their cholesterol. Maybe some of the thinking was the lower the better, which we'll come on to as well. So it doesn't matter what their cholesterol's starting from. The lower your cholesterol, the better. In fact, 2011, a cardiologist, one of the editors, I think, of the American Journal of Cardiology, wrote an article, which I mentioned in my book, A Statin-Free Life, which was entitled It's the Cholesterol, Stupid. Right? And what did he say in that? He said, you can be an obese diabetic smoker that doesn't exercise. Sounds crazy, but as long as your cholesterol is low enough, you're not gonna get heart disease.

You're not gonna get heart disease.

That's right.

Like, like really? So, okay. I had to unpick that. And, and, and what I, what I also then did moving forward from Suzanne Thode. So that's how I got down this track realizing that our obsession with LDL lowering has, has been a problem.

So you looked at the saturated fat literature and you weren't impressed and Data showed that it didn't seem to be both observational data and randomized controlled trials.

No benefit, like in lowering it, no association, nothing. Right, right. And then when you look at all the data, so that was the first sort of bit that I was okay.

And some might even been protective, like some of the dairy fat.

Well, we know now, yes, there is, there is some suggestion that dairy fat could be protective. Absolutely. So there's all that.

And then coming back to the LDL hypothesis, by the way, you're not alone on this. I mean, there was a major paper published by Darsh Mazafari from Tufts and others. Looking at butter and, and actually showing that there really wasn't evidence that it was harmful.

So Mark, this is what's interesting. That article I wrote, because creates such a, you know, a lot of headlines and, and then backlash or whatever else. That's when people like Darius started looking at this again. So it was all really from the back of that BMJ piece.

Yeah.

It all came together. Yeah. So then everybody's like, you know, I know, and at the time I was, I was writing just a, a commentary, which was peer reviewed, but I could have got it wrong. I could have.

Yeah.

But I was like, you know what? There's enough here that for me at least to provoke the thoughts. Right. And then it all got proven that, you know, what I'd written had validity, right?

Yeah.

Which is good. But the other aspect to this, if we go back and you mentioned cholesterol, so the, so is cholesterol, so for, is high cholesterol a risk factor for heart disease and is LDL cholesterol a risk factor for heart disease?

Yeah.

So you have to go back to square one, right? So these are the Framingham studies that, you know, started in Massachusetts in 1948 and went over decades looking at thousands of people where a lot of risk factors emerged for heart disease, whether it's diabetes, high blood pressure, smoking, for example. High cholesterol and high cholesterol, right? So you go and look back at the Framingham studies and what, and the, just to summarize it without complicating the situation too much, William Castelli is a cardiologist and he published, he was a co-director of Framingham. And in 1996 he published in one of the cardiology, major cardiology journals, a summary of Framingham, specifically looking at LDL cholesterol. Let's just, let's just look at LDL because that is the so-called bad cholesterol.. And he said from Framingham, unless your LDL was above 7.8 millimoles, which by the way, I think in your units is probably 250 or 300. Yeah. 250 probably. I think maybe we can look it up and calculate, but let's just say for argument's sake, around 250, which is very, very high by the way. It absolutely had no, it was useless as a predictor for coronary artery disease.

LDL.

LDL. Now why is that? When you correct for triglycerides and HDL, Okay. Which by the way is a more important predictor of heart disease. LDL loses its significance completely. So then if that's true, and I'm saying that means LDL isn't really a risk factor of heart disease, and I believe with everything I know now that to be the case, okay, let's, let's unpick every part of it. Does lowering LDL cholesterol from diet or drugs, but more specifically drugs cuz they're the most potent ways of lowering LDL cholesterol, whether it's PCK9 inhibitors, whether it's statins, whatever. Is the, is there a clear correlation? Is this dogma true that the lower the better? So myself and two cardiologists did a systematic review of the totality of drug industry sponsored trials, by the way, and some diet trials, but many drug industry sponsored trials, all of the randomized controlled trials on cholesterol lowering drugs, statins, PCK9, blah, blah, blah. Was there a clear relationship as you lowered LDL in low risk and high risk patients, Mark? Okay. Over 30 studies.

Yeah.

Was there a relationship with lowering LDL and preventing cardiovascular events? No. Even in high-risk patients, even in high risk, it's nonsense. It's nonsense. So the question then is, so why do we all so firmly believe? No. So does that mean statin? But then I said, well, of course statins have a role. They do have a benefit from the, from the RCT data, which is small because I knew already they're anti-inflammatory and anti-clotting. So it's nothing in my view. Listen, I could be proven wrong here, but the evidence at the moment looks very clear. That there is no consistent relationship, right? It's definitely not a clear relationship. So if, even if it's a weak relationship, Mark, let's just argument's sake, let's say there is a weak benefit in lowering LDL. What else is going on and what else are you ignoring? Right? Yeah. What else do statins do? They cause insulin resistance. Say 1 in 100 people get type 2 diabetes because of statins.

1 in 2, 1 in 100, 1 in 100.

Yeah. 1 in 100. So about 1 to 2%, but 1 in 100. Some, some studies say 1 in 50, right? We'll get type 2 diabetes because of the statin. Probably reversible still, but not ideal, right? If you're on a statin drug. The second thing is look at the whole patient coming in. We have the illusion of protection. We have patients I used to see coming in and they thought, my cholesterol is low, I can go and eat McDonald's, it's fine. And they, they're eat and they're, they're getting more and more overweight, more insulin resistant. They're increasing their cardiovascular risk. They're not told the statin is gonna give them a 1% benefit, i.e., more likely than not, they're not gonna benefit. So, you could imagine that concept that the overall net effect of the way that statins are prescribed and the dogma around them, in my view, has been negative and has actually been one of the main reasons why we have got this pandemic of chronic disease.

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Because there's a drug for it. It was interesting to me if there was a drug for insulin resistance that worked really well and we have metformin, but it's, eh, and it fixed insulin resistance. You know, everybody'd be prescribing it, but we don't even diagnose it in most people because we don't have a drug for it.

Exactly.

And it's, it's stunning to me that You know, I was talking to the lab director at Quest Laboratories. I said, what percent of your tests you get that come in are measuring insulin? Which is, I think, one of the most important things you need to know about your, yeah, biomarkers.

And he was like, less than 1%.

And then it's part of why I co-founded this company, Function Health, to really look at a deep biomarker set around cardiometabolic risk factors, including insulin, including Lp, including something called ApoB, which I wanna talk to you about.

Yeah.

Not just your total LDL, HDL, and triglyceride levels, but also particle number, particle size, inflammation markers, all the things that are often missed, but that are much better at giving you a holistic picture of your cardiovascular risk. And then you know where to intervene.

And it, in, in one of the studies that it was so interesting to me was actually from, I think Scotland or Ireland was where they looked basically at a series of patients who came into an emergency room with a heart attack.

And they did glucose tolerance tests on everybody who came in with a heart attack, and they found that two-thirds either had diabetes or pre-diabetes.

Yeah.

Who had a heart attack.

Yeah.

That, that was really the big driver.

Yeah.

Now there's a subset of people have familial lipid disorders, you know, inherited genetic lipid disorders, and not those people probably need to be treated more directly. But, but for the majority of people out there who are obese or have pre-diabetes or metabolic dysfunction, which is basically in America, 93% of Americans, That's what's driving probably most of the heart disease, not 100% butter or saturated fat or no, uh, LDL elevations. Yeah.

Well, something else to throw into the picture, right? So you can make the argument, okay, Dr. Malhotra, you're saying there's no consistent relationship. There may be a benefit. Why not just lower your LDL? Okay. So 2016, and the reason we did this, me and a number of international scientists looked at, we decided to do a systematic review of observational data looking at people over 60. Was there a relationship with LDL cholesterol and heart disease? And the reason we did this, by the way, is another thing that was interesting from Framingham, which wasn't well publicized, is that when, after people hit 50 years old, as their cholesterol dropped, their mortality increased.

Yeah.

So we thought, okay, is there something, you know, because for it to be a risk factor for heart disease, it should be consistent really across all age groups and both sexes, right?

For mortality.

For mortality. Yeah. But even for heart disease as well, right? You, that's a good point. So we looked at, was there first of all any association if you're over 60 with LDL cholesterol and heart disease, right? We found none. Okay. Interesting. But what was surprising was there was an inverse association with LDL cholesterol and all-cause mortality. In other words, statistically, if you're over 60, the higher LDL, the less likely you are to die. So what's the reasoning for that? Well, something that's been forgotten or missed or not discussed. Cholesterol is, has a very vital role in many functions in the body, including, you know, brain, the brain hormone production, but also the immune system.

Mm-hmm.

And it's likely that that's where the protective benefit comes because older people are more vulnerable to dying from infections. Yeah. And we also know there is an association. I'll use this word, an association, right? Can't say it's definitely causal between low cholesterol and cancer. Again, it's probably related to the immune system.

Yeah.

I mean, I think, I think the, which is very interesting.

The problem with this data though is, and I'll just push back a little bit, is it's, it's observational data.

Yeah.

And the data.

Like from the Hawaii study show that, you know, the, you were older and you had higher cholesterol, you know, you're more likely to live longer than if your cholesterol's lower.

Yeah.

But it may be because the people had low cholesterol are malnourished, have cancer and other reasons.

So let me push back on that. So we, we counted for that and we found actually no, when you, you account like time lag, you go back 5 or 10 years. No, it's not, it's not the, it, that does happen, but it, no, it's independently, it does seem to be an issue.

Okay. So you sort of looked at all the data and you came up with this very kind of contrary opinion, which is that LDL isn't all it's cracked up to me, that statins work a little.

Yeah.

But not for the reasons we think. Meaning they lower inflammation and they may have other properties that may be beneficial. We don't even know what to call this pleiotropic effects. So they, for example, they induce nitric oxide synthase, which dilates your blood vessels and reduces inflammation and helps your lining of your blood vessels. All that's protective. And so it may be, it stabilizes plaque, it may help in those ways, but it may not be the LDL lowering effect. In fact, Paul Ridker from Harvard, I remember he published a trial, I think it was the Jupiter trial where they showed that if you, if you had a high LDL but didn't have any inflammation, you didn't have that significant a risk of having heart disease. But if you had interesting, a high level of inflammation, high LDL, you had a much higher risk. So it was the inflammation that was really driving the heart disease. And that was really the seminal paper was in the New England Journal of Medicine over 20 years ago. I remember reading it.

Yeah.

By Paul Ridker and, and his crew that really laid out how, Heart disease is not a plumbing problem, it's an immune problem.

100%. It's a chronic inflammatory process exacerbated by metabolic risk factors or insulin resistance.

And I wrote a metabolic risk factors. By that you mean problems with your blood sugar and insulin, insulin resistance and prediabetes.

100%. And actually we published an editorial with two cardiologists I did in British Journal of Sports Medicine in 2017, which was a very long title, but it got a lot of publicity and over more than a million downloads, which was, um, Saturated fat does not clog the arteries. Coronary artery disease is a chronic inflammatory condition, which can be effectively managed with lifestyle changes. That was the title of this thing. But it's all there, people, it's free access. People can look it up and read it. But we talk that we've overdone the thing. And it wasn't just Dr. Malhotra, his opinion being controversial. The two, my two co-authors were both editors of medical journals and cardiologists, Louis Redberg, editor of JAMA Internal Medicine, and Pascal Meyer, editor of BMJ Open Heart.

So why is this not getting more play?

Why is still the dogma And the orthodoxy that if you have a high LDL, you take a statin.

Do, do you want my honest answer, Mark?

Yeah. I mean, not, not all, I mean, I, I know doctors are usually very good-hearted.

Sure.

Very smart. Well-intentioned. Don't wanna hurt their patients.

Try to do what's in the best interest of their patients and follow the science.

So why, why are they not hearing about this?

Okay, so let's go to the root cause of the problem. Even in society today, what's the big issue in health? We have commercial distortions of the scientific evidence. Who's behind that and who has more power and control over medical education, medical training, the media than ever before? Big corporations, in this case, big pharma. And the level of this control and power, Mark, has got to a level where it can be very easily and rationally, not in an inflammatory way or overplaying it as being tyrannical, What also happens with these big corporations in the way they exert their power is that they want to avoid conflict, right? They want to avoid the truth coming out. So there's a debate and discussion because ultimately people like myself, like you, who are obsessed with the truth, who want to get it out to help patients, when we speak and act from a place of integrity and truth, It has a very powerful resonance with people and it can very quickly destroy all these other dogmas that people have created because of that power that the truth has. They want that conflict to remain latent, to remain hidden so that, you know, Noam Chomsky says the general public doesn't know what's happening and they don't even know that they don't know. That's right. Right. So a lot of these doctors, and I agree, are well-intentioned, but they don't, they're living, you know, in many ways they're living, uh, they're climbing up the wrong wall. To success when it comes to helping patients.

Mm-hmm.

Because it's the drug companies that are, are really calling the shots. Yeah. So we are under a situation of tyranny, and the reason I call it tyrannical is because there are doctors that know this, uh, Mark, there are a few doctors that kind of know this, but then they're less, they're afraid to speak out. And only a minority of the doctors that know what's going on will then speak out.

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